Save Our Monkeys counters claims made for using Mauritius macaques in Hepatitis B research

Save Our Monkeys counters claims made for using Mauritius macaques in Hepatitis B research

20/06/2014

The BUAV Save Our Monkeys campaign aims to raise awareness of the plight of the long-tailed macaque in Mauritius and urges the people of Mauritius to support the BUAV’s efforts to stop the cruel trade and export of monkeys around the world for use in experiments. There are strong ethical and scientific arguments against their use in research.

A recent paper by Dupinay et al. (1)describes the first identification of naturally occurring chronic hepatitis B virus infection in an old world monkey, in this case long-tailed macaques living in Mauritius. The authors propose that these macaques could be used for the study of hepatitis B infection and related disease in humans.

The BUAV disagrees with this approach for the following reasons:

There are already several successful preventive Hep B vaccines for humans. To address valid concerns over the impact of Hep B across the world in spite of the existence of these vaccines, improvements in vaccination programmes is an obvious area for attention.

There are several treatments available for people infected with hepatitis B. These can be very effective, though efficacy depends on the type of Hep B virus and individual responses.

Using animals is unlikely to be helpful, and most likely to be misleading due to poor human relevance. For example, the chimpanzee — much more closely related to humans than the macaque — was touted for many years as being crucial for Hep C and HIV/AIDS research and the quest for vaccines for those viruses, but is no longer used due to major species differences, and failures, leading to it being considered ‘unnecessary.’

There are already known species differences that should serve as a warning that using the long-tailed macaque would be of poor human relevance. For example, the virus in these monkeys is of a very specific type, which is only found in specific populations of humans, and which has different properties, such as ensuing pathology/course and severity of infection, response to interventions etc., from other types. Further, there is a specific genetic polymorphism (mutation) in this monkey virus, which seems essential for its infectivity in the monkeys: the monkeys’ liver cells were not able to be infected with a human Hep B virus (HBV). Another important difference is acknowledged by the authors in this paper: ‘Whereas HBV causes liver disease in humans, this virus generally produces only a benign infection in primates.’

Research efforts are focussed primarily on an understanding of the Hep B virus life cycle, and on the discovery of treatments that are better, and which have fewer side effects, than those currently available. Crucially, the argument that a small-animal ‘model’ is necessary for this is weak, as many alternative approaches are widely used and highly productive.

Save Our Monkeys argues that alternative methods that do not involve the use of animals should be used instead and points to those that have been published within the last few months alone:

Improvements in cell culture methods to make human liver cells (susceptible to HBV infection for study) longer lasting and more appropriate to the in vivo situation (2).